Evidence map›Paper›PMID 22355653›Full record

ArticleScientific reports2011

Inactivation of CBF/NF-Y in postnatal liver causes hepatocellular degeneration, lipid deposition, and endoplasmic reticulum stress.

Rong Luo, Sherry A Klumpp, Milton J Finegold, Sankar N Maity

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Journal of medicinal chemistry · 2026
    Article
  2. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC).International journal of molecular sciences · 2020
    Article
  8. Article
  9. NF-Y (CBF) regulation in specific cell types and mouse models.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Rong LuoDepartment of Molecular Genetics, The University of Texas, M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Sherry A Klumpp
Milton J Finegold
Sankar N Maity
Texas Children's Hospital · USThe University of Texas at Austin · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tissue Analysis & Molecular Imaging CoreP30DK056338 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI Geoffrey A Preidis · 2001 to 2026
$28.3M
ROLE OF CBF/NF-Y IN TRANSCRIPTION: TYPE I COLLAGEN GENESR01AR046264 · NIAMS · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI MAITY, SANKAR N · 2000 to 2004
$1.3M
NCI NIH HHS CA 16672NCI NIH HHS P30 CA016672NIAMS NIH HHS R01 AR046264NIAMS NIH HHS R01 AR46264NIDDK NIH HHS P30 DK056338NIDDK NIH HHS P30 DK56338
6 · The paper itself

Abstract

We previously demonstrated that CBF activity is needed for cell proliferation and early embryonic development. To examine the in vivo function of CBF in differentiated hepatocytes, we conditionally deleted CBF-B in hepatocytes after birth. Deletion of CBF-B resulted in progressive liver injury and severe hepatocellular degeneration 4 weeks after birth. Electron microscopic examination demonstrated pleiotropic changes of hepatocytes including enlarged cell and nuclear size, intracellular lipid deposition, disorganized endoplasmic reticulum, and mitochondrial abnormalities. Gene expression analyses showed that deletion of CBF-B activated expression of specific endoplasmic reticulum (ER) stress-regulated genes. Inactivation of CBF-B also inhibited expression of C/EBP alpha, an important transcription factor controlling various metabolic processes in adult hepatocytes. Altogether, our study reveals for the first time that CBF is a key transcription factor controlling ER function and metabolic processes in mature hepatocytes.

Indexed as

AnimalsAnimals, NewbornCCAAT-Binding FactorEndoplasmic Reticulum StressFatty LiverGene ExpressionHepatocytesHepatomegalyLipid MetabolismLiverMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, Electron, TransmissionCCAAT-Binding Factor

Identifiers

PMID22355653
PMCPMC3216617
OpenAlexW1981537690

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.